Abstract
Triglyceride to high-density lipoprotein cholesterol (TG/HDL-C) ratio and the triglyceride-glucose (TyG) index have become novel and convenient indicators of insulin resistance (IR) and are reported to be associated with occurrence and prognosis of myocardial infarction (MI). Mean arterial pressure (MAP) is another MI indicator that affects myocardial perfusion and oxygen delivery. However, the association between TG/HDL-C ratio and TyG index with MAP in patients with MI remains unclear. The purpose of this study was to explore the correlation between TG/HDL-C ratio and TyG index with MAP in patients with MI, which may provide valuable insights for the clinical assessment and management of MI patients. A total of 7341 patients with MI from January 2019 to December 2020 were enrolled to collect the general clinical data. Univariate and multivariate linear regression analyses were employed to examine the relationships between TG/HDL-C ratio and TyG index with MAP. Generalized additive models (GAM) and threshold effects analysis were applied to explore dose-response patterns. Gender and age interactions were tested. The average age of the 7341 patients with MI was 61.39 ± 13.13, and 62.23% were male. Both TG/HDL-C ratio and TyG index were positively associated with MAP. GAM analysis revealed that TG/HDL-C ratio showed non-linear associations with a threshold at 1.43, while TyG index demonstrated consistent linear relationships. Below the threshold, each unit increase in TG/HDL-C ratio was associated with 2.23 mmHg increase in MAP (95%CI: 0.76–3.71, P = 0.0029); above threshold, associations were attenuated (P = 0.2021). TyG index showed linear association throughout its range (β = 0.30, 95%CI: 0.16–0.44, P < 0.0001). Both markers demonstrated stronger associations in male patients (P for interaction = 0.027). TG/HDL-C ratio and TyG index were positively associated with MAP in MI patients, showing threshold-based and linear patterns respectively. Both markers exhibited stronger associations in males. Monitoring these IR markers with consideration of threshold effects and gender differences deserves attention in clinical practice for MI management.
Introduction
Acute myocardial infarction (AMI) is a global disease with high morbidity and mortality worldwide, which seriously affects the quality of patients’ life1. Based on the coronary atherosclerosis, AMI is caused by secondary plaque rupture and thrombosis, which leads to sustained and complete blockage of coronary arteries and severe acute ischemia of the corresponding myocardium. Despite percutaneous coronary intervention (PCI) has largely improved the mortality and complications of AMI, it is still very necessary to find new risk assessment indicators to further evaluate and predict the risk and prognosis of AMI patients.
Disorder of lipid metabolism and glucose metabolism are two of the key metabolic abnormalities involved in atherosclerosis and myocardial infarction (MI). At present, insulin resistance(IR) is considered to be an important pathophysiological basis for the occurrence and development of dyslipidemia, type 2 diabetes, hypertension and atherosclerosis2. Studies has confirmed the correlation between IR and the severity and prognosis of coronary atherosclerosis3. The gold standard for evaluating IR is the hyperinsulinaemic-euglycaemic clamp(HEC) test, but features such as invasiveness, complexity, and high expense limits its widespread clinical application4,5.
The triglyceride (TG) to high-density lipoprotein cholesterol (HDL-C) (TG/HDL-C) ratio and the triglyceride-glucose (TyG) index have become novel and convenient indicators of IR in recent years. TG/HDL-C ratio is an independent influencing factor and an effective predictor of IR, and its predictive value on IR is stronger than that of simple TG and HDL-C6. Besides, elevated TG/HDL-C ratio is associated with coronary heart disease, metabolic syndrome, diabetes and arterial stiffness7,8. TyG index involves TG and fasting blood glucose(FBG), meaning it can combine two classic risk factors of coronary atherosclerosis disease, glucose metabolism and lipid metabolism, to better reflect IR with satisfactory sensitivity and specificity9, and has predictive role for atherosclerosis10, MI11 and coronary artery disease12. And TyG index was sight to be a marker in cardiovascular disease(CVD)13.
Mean artery pressure (MAP) is the result of a combined response of the cardiovascular and neuroendocrine system and is considered a stabilizing component of blood pressure that fluctuates between systolic pressure and diastolic pressure (SBP and DBP). MAP affects myocardial perfusion and oxygen delivery, and high levels of MAP are significantly associated with total mortality and cardiovascular mortality in patients with AMI14,15. Moreover, in post-cardiac arrest patients with shock after AMI, targeting MAP between 80/85 and 100 mmHg was associated with less myocardial injury16. Thus, maintaining an appropriate level of MAP is of crucial clinical importance for patients with MI.
The relationship between IR and blood pressure has garnered increasing interest among researchers. Several studies have indicated that the TG/HDL-C ratio serves as a valuable predictor of hypertension17. Furthermore, the TyG index and TG/HDL-C may serve as potential indicators for the progression of arterial stiffness and hypertension18,19. However, the association between IR and MAP in patients with MI is remains uncertain, especially the relationships between TG/HDL-C ratio and TyG index with MAP is rarely reported. Consequently, we conducted a cross-sectional study to elucidate the correlation between the TG/HDL-C ratio and TyG index with MAP in patients with MI, aiming to provide additional empirical support for the early assessment and prognosis of MI.
Methods
Study design and participants
This was a single-center, observational cross-sectional study. Patients diagnosed with MI from January 2019 to December 2020 were retrospectively collected from the biobank of the First Affiliated Hospital of Xi ‘an Jiaotong University. MI included acute, chronic MI and old MI. The inclusion criteria were: ① All patients met the diagnostic criteria for MI in the “Fourth General Definition of Myocardial Infarction” proposed by the executive panel of the Joint European Society of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA)/World Heart Federation (WHF)20; ② All patients underwent coronary angiography. The exclusion criteria were: ① malignant tumor; ② severe hepatic and renal insufficiency; ③ immunity from systemic diseases; ④recent acute and chronic infectious diseases; ⑤ loss of TG, HDL-C and fasting glucose (FPG) values.
The current study was carried out in accordance with the Declaration of Helsinki and approved by the Ethics Committee of the First Affiliated Hospital of Xi’an Jiaotong University (Ethical approval number: XJTU1AF2021LSK-450).
Clinical data collection
Baseline characteristics, including demographic data, laboratory tests, primary diagnosis, and discharge medication were collected. Traditional cardiovascular risk factors, including age, sex, SBP, DBP were collected within 24 h after admission. Total cholesterol (TC), TG, HDL-C, low-density lipoprotein cholesterol (LDL-C), FPG, high-sensitivity cardiac troponin T (hs-cTnT), N-terminal prohormone of brain natriuretic peptide (NT-proBNP), creatinine, glycosylated hemoglobin A1c (HbA1c), albumin, aspartate aminotransferase (AST), alanine transaminase (ALT), white blood cell (WBC), platelet and hemoglobin were obtained from fasting venous blood samples at admission or the following morning. The TG/HDL-C ratio = TG(mg/dL)/HDL-C(mg/dL); TyG = Ln [fasting TG (mg/dL) × FPG (mg/dL)/2]21. The MAP at admission was calculated as 1/3 (admission SBP) and 2/3 (admission DBP) and rounded to the nearest whole number. Admission SBP and DBP were defined as SBP and DBP in the supine or seated position first recorded after admission to the ward. All of these laboratory tests were implemented using standard methods.
Statistical analysis
The 7341 MI patients were classified into quartiles based on TG/HDL-C ratio and TyG index values at hospital admission, with Q1 representing the lowest and Q4 the highest values. For TG/HDL-C ratio: Q1 (n = 1835), Q2 (n = 1835), Q3 (n = 1834), and Q4 (n = 1837). For TyG index: Q1 (n = 1820), Q2 (n = 1823), Q3 (n = 1823), and Q4 (n = 1822). The specific quartile ranges and median values for each group are presented in the respective tables.
SPSS26.0 statistical software was used for data processing and statistical analysis. Continuous variables are presented as median (lower quartile, upper quartile). Categorical variables are presented as numbers and percentages. Given the large sample size and to avoid assumptions about normality, the Kruskal-Wallis H test was consistently used for all continuous variable comparisons among groups, and the chi-square test was used for categorical variables. The association between TG/HDL-C ratio and TyG index with MAP values was evaluated by univariate and multivariate linear regression analysis. The TG/HDL-C ratio and TyG index were both analyzed as continuous variables and categorized into quartiles respectively. In multivariate linear regression analysis, Model 1 adjusted for age and gender; Model 2 adjusted for age, gender, cholesterol, hs-cTnT, NT-proBNP, HbA1c, albumin, WBC, platelet and creatinine. To explore dose-response relationships without assuming specific functional forms, we implemented generalized additive model (GAM) to investigate the relationship between TG/HDL-C ratio and TyG index with MAP. Threshold effect analysis was performed using two-piecewise linear regression models with automatic turning point detection. Likelihood ratio tests (LRT) were used to determine the statistical significance of threshold effects by comparing single-line versus two-piecewise regression models. Values exceeding the 99th percentile for TG/HDL-C ratio and TyG index were treated as missing data to minimize the influence of extreme outliers while preserving the underlying data distribution.
The interactive terms were tested in the model to identify the interaction of TG/HDL-C ratio and TyG index with gender and age. To assess the robustness of interaction effects, analyses were performed using both the original complete dataset and after treating extreme values. Additionally, GAM with gender- and age-specific smooth curve fitting were applied to visualize dose-response relationships and provide assumption-free validation of linear regression interaction findings. All the P-values were two-sided tests, and the test level was α = 0.05, using P < 0.05 was considered statistically significant.
Results
Basic characteristics of the participants according to quartile of TG/HDL-C ratio
The study included total 7341 patients diagnosed with MI, with an average age 61.39 ± 13.13 years. Among these patients, 62.23% were male. Table 1 presents the baseline characteristics of all participants categorized into quartiles based on the TG/HDL ratio. Various parameters including proportion of males, SBP, DBP, MAP, TG, cholesterol, LDL-C, hs-cTnT, FPG, creatinine, HbA1c, albumin, ALT, WBC, platelet, and hemoglobin showed a significant increase with increasing quartiles of the TG/HDL-C ratio (all P < 0.05). While age and HDL-C were decreased as quartiles of TG/HDL-C ratio increased (all P < 0.05). Notably, the Q2 group of TG/HDL-C exhibited the highest levels of NT-proBNP and lowest levels of AST (all P < 0.05). The distribution and variations of MAP among the four group are depicted in Fig. 1A. The levels of MAP increased progressively across TG/HDL-C quartiles (P < 0.05).
Basic characteristics of the participants according to quartile of TyG index
The baseline characteristics of all participants by quartiles of the TyG index are presented in Table 2. SBP, DBP, MAP, TG, cholesterol, LDL-C, hs-cTnT, FPG, creatinine, HbA1c, albumin, AST, ALT, WBC, platelet and hemoglobin were increased with quartiles of TyG index (all P < 0.05). While age, HDL-C and NT-proBNP decreased with quartiles of TyG index (all P < 0.05). There had no statistical difference of gender among the four groups. The distributions and difference of MAP among the quartile groups according to the TyG index are shown in Fig. 1B. Similarly, MAP levels increased progressively across TyG index quartiles (P < 0.05).
Association between insulin resistance markers and MAP
Table 3 presents the results of univariable and multivariable linear regression analyses examining the associations between TG/HDL-C ratio, TyG index and MAP after extreme value treatment. In univariable analysis, both TG/HDL-C ratio and TyG index showed significant positive associations with MAP. After full adjustment (Model 2), these associations remained significant: each unit increase in TG/HDL-C ratio was associated with a 0.82 mmHg increase in MAP (95% CI: 0.36–1.27, P = 0.0005), while each unit increase in TyG index was associated with a 0.30 mmHg increase in MAP (95% CI: 0.16–0.44, P < 0.0001). For quartile analysis, compared to the reference group (Q1), the highest quartiles showed significant associations with MAP in the fully adjusted model: TG/HDL-C Q4 was associated with 2.43 mmHg higher MAP (95% CI: 1.13–3.72, P = 0.0002), and TyG index Q4 with 1.71 mmHg higher MAP (95% CI: 0.30–3.13, P = 0.0179). A dose-response relationship was observed across quartiles for both indictors. Sensitivity analysis using original data without extreme value treatment yielded consistent results (Table S1), confirming the robustness of these associations.
Dose-response relationships and threshold effects
Figure 2 illustrates the associations between insulin resistance markers and MAP after extreme value treatment by GAM analysis. For TG/HDL-C ratio, GAM analysis revealed a non-linear relationship with MAP (Fig. 2A). The curve showed a steeper slope at lower values, with the relationship appearing to plateau at higher ratios. Threshold effect analysis (Table 4) confirmed this non-linear pattern, identifying an optimal turning point (K) at TG/HDL-C ratio = 1.43. Below this threshold, each unit increase in TG/HDL-C ratio was associated with a substantial 2.23 mmHg increase in MAP (95% CI: 0.76–3.71, P = 0.0029), while above the threshold, the association was attenuated and non-significant (β = 0.40, 95% CI: −0.21-1.01, P = 0.2021). The likelihood ratio test confirmed that the two-piecewise linear model was significantly superior to the single linear model (P = 0.046), indicating a true threshold effect rather than a linear relationship.
In contrast, TyG index demonstrated a consistent linear relationship with MAP throughout its range (Fig. 2B). Threshold effect analysis supported this linear pattern, as the likelihood ratio test showed no significant difference between linear and non-linear models (P = 0.245), indicating no threshold effect and confirming that the single linear model adequately describes this relationship. Sensitivity analysis using original data yielded consistent patterns (Figure S1), reinforcing the robustness of these dose-response relationships.
Dose-response relationships between insulin resistance markers and MAP using generalized additive models*. (A) Non-linear relationship between TG/HDL-C ratio and MAP with threshold effect. (B) Linear relationship between TyG index and MAP. Red lines represent estimated values with 95% confidence intervals (blue lines). Adjusted for gender, age, cholesterol, hs-cTnT, NT-proBNP, HbA1c, albumin, WBC, platelet, and creatinine. * Values > 99th percentile were treated as missing data.
Subgroup analysis and interaction effects
To explore potential effect modification, we performed subgroup analyses stratified by gender and age, with formal interaction testing. Analysis using the complete dataset showed borderline gender interaction for TG/HDL-C ratio (P = 0.061) and significant interaction for TyG index (P = 0.023), as detailed in Supplementary Table S2.
After extreme value treatment, both markers demonstrated significant gender interactions (Table 5). For TG/HDL-C ratio, the association with MAP showed clear gender-specific effects (P for interaction = 0.027), with significant effects in males (β = 0.95, 95% CI: 0.38–1.52, P = 0.0012) but not females (β = 0.34, P = 0.3938). Age-related interactions remained non-significant (P for interaction = 0.558). TyG index maintained significant gender interaction (P for interaction = 0.027), with substantially stronger associations in males compared to females (β = 0.35, 95% CI: 0.17–0.53, P = 0.0001 vs. β = 0.18, P = 0.1121). Age interaction was non-significant (P for interaction = 0.189), though effects were more pronounced in older patients (β = 0.43 vs. 0.12).
Figure 3 illustrates these subgroup-specific dose-response relationships using GAM analysis. The non-linear pattern of TG/HDL-C ratio with MAP was preserved across subgroups (Panels A and B), while the linear relationship of TyG index showed more pronounced slopes in male and younger patients (Panels C and D), supporting the quantitative interaction findings.
Subgroup analysis of relationships between insulin resistance markers and MAP using generalized additive models*. (A) TG/HDL-C ratio stratified by gender. (B) TG/HDL-C ratio stratified by age. (C) TyG index stratified by gender. (D) TyG index stratified by age. Red lines represent male/≥65 years, cyan lines represent female/<65 years. All models adjusted for gender, age, cholesterol, hs-cTnT, NT-proBNP, HbA1c, albumin, WBC, platelet and creatinine. * Values > 99th percentile were treated as missing data.
Discussion
In this cross-sectional study, we discovered significant associations between the TG/HDL-C ratio and TyG index with MAP levels in patients diagnosed with MI. The TG/HDL-C ratio demonstrated a non-linear association with MAP featuring a threshold at 1.43, while the TyG index showed a consistent linear relationship through its range. Notably, both markers exhibited stronger associations in male patients, with significant gender interactions for both. To the best of our knowledge, this is the first study to characterize these threshold-based and gender-specific associations between the TG/HDL-C ratio and the TyG index with MAP in the context of MI.
CVD remains the primary cause of morbidity and mortality worldwide22. There is a gradual increase in the burden of cardiometabolic risks such as hypertension, elevated LDL-C, higher BMI, increased FBG, and renal insufficiency. Furthermore, emerging evidence suggests that MAP holds significant value in evaluating the severity and prognosis of patients with AMI23. The TG/HDL-C ratio and TyG index have been developed as novel, simple and convenient assessment to identify IR with or without diabetes9,24. IR is not only the common pathophysiological basis of many chronic diseases25, but also an important predictor of CVD both in diabetic and nondiabetic subjects3. IR triggers imbalance of glucose metabolism, which contribute to hyperglycaemia, and inflammation and oxidative stress step by step26. In addition, elevated MAP can lead to endothelial dysfunction, reduces peripheral blood flow, affects insulin delivery, and promotes IR27. Conversely, an elevated MAP can contribute to the progression of atherosclerosis and arterial stiffness, resulting in compromised microcirculation hindered insulin delivery to target tissues, affecting glucose metabolism and leading to diabetes. These results suggest that the interaction between IR and hypertensive status might contribute to MI. Our study findings align with previous research18, which demonstrated that increased TyG index and TG/HDLC levels were linked to prehypertension and hypertension in normoglycemic individuals. Additionally, the TyG index exhibited greater significance than TG/HDL-C in distinguishing hypertension. Consequently, it is imperative to prioritize the assessment of IR indexes and MAP in the context of MI.
Dyslipidemia, characterized by elevated levels of TG and LDL-C, as well as reduced levels of HDL-C, has been found to be independently associated with MI, hypertension of other cardiometabolic risk factors28,29,30. Specifically, the TG/HDL-C ratio has been identified as a simple and useful indicator for identifying individuals with apparently healthy IR and those at an increased risk of cardiometabolic complications31. Several studies have demonstrated the effectiveness of the TG/HDL-C ratio as a predictor of hypertension17,32. A cross-sectional study conducted on men aged 10–26 years revealed that those with the highest TG/HDL-C levels exhibited elevated SBP and DBP33. Additionally, a prospective cohort study demonstrated a higher prevalence of hypertension in early adulthood compared to adolescents in the low TG/HDL-C ratio group17. Furthermore, Chung et al.34 found an independent and positive association between the TG/HDL-C ratio and arterial stiffness in postmenopausal Korean women. Similarly, a cross-sectional study involving Taiwanese adults indicated an increase in MAP across the TG/HDL-C quartiles35.
The TyG index, due to its consistent association with IR, has been identified as an independent predictor of hypertension36. Recent research37 has demonstrated a positive dose-response relationship between the TyG index and blood pressure. A cross-sectional survey conducted among Chinese adults38 found a significant association between elevated TyG index and an increased risk of prehypertension and hypertension. Wang et al.39 revealed a correlation between a high TyG index and greater arterial stiffness, as well as a correlation between the TyG index with SBP and pulse pressure. These findings suggest that the TyG index may serve as a reliable indicator for risk assessment and prognosis of T2DM and AMI40,41. Another study demonstrated that a combination of low TyG index and low SBP was linked to a reduced risk of all-cause and cardiovascular mortality42. These studies collectively highlight the potential of TyG index as a valuable tool for predicting hypertension and CVD. Nevertheless, limited research has explored the association between the TyG index and MAP in patients with MI. The present study posited that the TyG index exhibits a positive relationship with MAP in patients with MI. These findings expand the importance of evaluating the TG/HDL-C ratio and TyG index in relation to MAP, thereby offering novel evidence for the assessing the severity of MI.
The implementation of GAM and threshold effect analysis revealed distinct dose-response relationships that were previously obscured by traditional linear modeling approaches. GAM analysis demonstrated clear non-linear patterns for TG/HDL-C ratio with saturation effects, while confirming predominantly linear relationships for TyG index throughout its entire range. Threshold effect analysis identified a critical turning point at TG/HDL-C ratio = 1.43, where the relationship with MAP fundamentally changes from a steep association below the threshold to an attenuated pattern above it. Importantly, these findings remained robust across sensitivity analyses, confirming the biological validity of these dose-response patterns. The threshold discovery for TG/HDL-C ratio provides new insights into the pathophysiology of lipid-mediated insulin resistance in MI patients. Below the threshold, the steep dose-response relationship suggests maximal vascular sensitivity to triglyceride and HDL-cholesterol imbalances. Above this threshold, the relationship plateaus, potentially due to saturation of compensatory mechanisms. This saturation pattern may explain why some patients with extremely elevated TG/HDL-C ratios do not show proportionally severe cardiovascular manifestations. In contrast, the consistent linear relationship observed for TyG index indicates that glucose-mediated insulin resistance pathways maintain their dose-response relationship without apparent saturation effects, suggesting fundamentally different regulatory mechanisms.
Both insulin resistance markers demonstrated significant gender interactions, with consistently stronger associations observed in male MI patients. These gender-specific associations observed in our study align with some previous research demonstrating stronger effects in males. A cross-sectional study on Taiwanese adults found that higher TG/HDL-C ratio was associated with cardiovascular risk factors exclusively in males35, while a prospective study demonstrated that elevated TC/HDL-C ratios were independently linked to hypertension risk in males28. However, conflicting results exist, with some studies showing stronger associations in females43,44. Additional research45 suggests that estrogens-related pathways may play a role, emphasizing the importance of subgroup analyses considering menopausal status46.
To understand the underlying biological basis for these gender-specific associations, several mechanistic pathways warrant consideration. The stronger associations between insulin resistance markers and MAP observed in male MI patients can be attributed to interconnected biological mechanisms. Hormonal influences play a crucial role: testosterone promotes visceral adiposity and enhances pro-inflammatory cytokine production, directly impairing insulin signaling pathways and vascular reactivity47. In contrast, estrogen in premenopausal women provides cardiovascular protection through enhanced nitric oxide bioavailability and improved endothelial function48. Gender differences in body fat distribution significantly contribute, with males exhibiting preferential visceral adiposity patterns that secrete higher levels of pro-inflammatory adipokines while producing lower protective adiponectin levels49. This creates a more pronounced inflammatory milieu contributing to insulin resistance and sympathetic activation. Additionally, males demonstrate greater insulin-mediated vasoconstriction and reduced endothelium-dependent vasodilation, making them more susceptible to the hypertensive effects of insulin resistance markers50.
The strength of the present study included the large sample size, implementation of statistical methodologies including GAM and threshold effect analysis, and comprehensive sensitivity analyses that provide cross-sectional data on the association between the TG/HDL-C ratio and TyG index with MAP in MI patients. The robust analytical approach, including extreme value treatment and multiple model validation, enhances the reliability of our findings. The present findings have several potential clinical implications. These easily calculated indices could serve as additional risk assessment tools for identifying MI patients with elevated MAP and warrant closer monitoring. The associations observed suggest that metabolic management, particularly targeting insulin resistance, might be an important consideration in comprehensive MI care. Given their convenience and cost-effectiveness from routine laboratory parameters, these indices could be readily integrated into existing clinical workflows for risk stratification.
There are several limitations to this study. First, although key clinical and laboratory variables were systematically adjusted, some unmeasured confounding factors such as lifestyle patterns, psychosocial factors, and genetic variations might still affect the results, representing an inherent limitation of cross-sectional studies. Second, we only recorded baseline MAP and failed to collect hypotensive drug use, dynamic changes, volatility, or cumulative levels might provide more valuable clinical indications. Thirdly, this single-center study requires validation in larger, multi-regional studies. Lastly, the cross-sectional design lacks follow-up data, and further studies are needed to determine whether the TG/HDL-C ratio and TyG index have an impact on long-term prognosis and mortality in MI patients.
Conclusion
In summary, TG/HDL-C ratio and TyG index were positively associated with MAP in MI individuals. The present study revealed important threshold-based relationships for TG/HDL-C ratio (threshold at 1.43) and consistent linear relationships for TyG index, with significant gender-specific patterns demonstrating stronger associations in male patients. Therefore, monitoring the TG/HDL-C ratio and TyG index with consideration of threshold effects and gender-specific patterns deserves more attention in clinical practice for the early prevention and prognosis of MI.
Data availability
The datasets used in this study are available from the corresponding author on reasonable request.
References
Palasubramaniam, J., Wang, X. & Peter, K. Myocardial Infarction-From atherosclerosis to thrombosis. Arterioscler. Thromb. Vasc Biol. 39, e176–e185 (2019).
Laakso, M. & Kuusisto, J. Insulin resistance and hyperglycaemia in cardiovascular disease development. Nat. Rev. Endocrinol. 10, 293–302 (2014).
Tao, L-C., Xu, J-N., Wang, T-T., Hua, F. & Li, J-J. Triglyceride-glucose index as a marker in cardiovascular diseases: landscape and limitations. Cardiovasc. Diabetol. 21, 68 (2022).
Minh, H. V. et al. Assessment of preferred methods to measure insulin resistance in Asian patients with hypertension. J. Clin. Hypertens. (Greenwich). 23, 529–537 (2021).
Muniyappa, R., Lee, S., Chen, H. & Quon, M. J. Current approaches for assessing insulin sensitivity and resistance in vivo: advantages, limitations, and appropriate usage. Am. J. Physiol. Endocrinol. Metab. 294, E15–26 (2008).
Kim-Dorner, S-J., Deuster, P. A., Zeno, S. A., Remaley, A. T. & Poth, M. Should triglycerides and the triglycerides to high-density lipoprotein cholesterol ratio be used as surrogates for insulin resistance? Metabolism 59, 299–304 (2010).
Vega, G. L., Barlow, C. E., Grundy, S. M., Leonard, D. & DeFina, L. F. Triglyceride–to–High-Density-Lipoprotein-Cholesterol Ratio is an Index of Heart Disease Mortality and of Incidence of Type 2 Diabetes Mellitus in Men. J Invest Med [Internet]. [cited 2023 Dec 24];62:345–9. Available from: http://journals.sagepub.com/doi/ (2014). https://doi.org/10.2310/JIM.0000000000000044
Hadaegh, F. et al. Triglyceride/HDL-cholesterol ratio is an independent predictor for coronary heart disease in a population of Iranian men. Nutr Metab Cardiovas [Internet]. [cited 2023 Dec 24];19:401–8. (2009). Available from: https://linkinghub.elsevier.com/retrieve/pii/S0939475308001877
Guerrero-Romero, F. et al. The product of triglycerides and glucose, a simple measure of insulin sensitivity. Comparison with the euglycemic-hyperinsulinemic clamp. J. Clin. Endocrinol. Metab. 95, 3347–3351 (2010).
Irace, C. et al. Markers of insulin resistance and carotid atherosclerosis. A comparison of the homeostasis model assessment and triglyceride glucose index. Int. J. Clin. Pract. 67, 665–672 (2013).
Kim, M. K. et al. Relationship between the triglyceride glucose index and coronary artery calcification in Korean adults. Cardiovasc. Diabetol. 16, 108 (2017).
Cho, Y. K. et al. Triglyceride Glucose-Waist circumference better predicts coronary calcium progression compared with other indices of insulin resistance: A longitudinal observational study. J. Clin. Med. 10, 92 (2020).
Tao, L-C., Xu, J., Wang, T., Hua, F. & Li, J-J. Triglyceride-glucose index as a marker in cardiovascular diseases: landscape and limitations. Cardiovasc Diabetol [Internet]. [cited 2023 Dec 24];21:68. Available from: https://cardiab.biomedcentral.com/articles/ (2022). https://doi.org/10.1186/s12933-022-01511-x
Avanzini, F. et al. High pulse pressure and low mean arterial pressure: two predictors of death after a myocardial infarction. J. Hypertens. 24, 2377–2385 (2006).
Kengne, A-P. et al. Blood pressure variables and cardiovascular risk: new findings from ADVANCE. Hypertension 54, 399–404 (2009).
K A, P J, J H, M R, V P, P L, et al. Optimum Blood Pressure in Patients With Shock After Acute Myocardial Infarction and Cardiac Arrest. Journal of the American College of Cardiology [Internet]. [cited 2024 Jan 30];76. (2020). Available from: https://pubmed.ncbi.nlm.nih.gov/32792079/
Yeom, H., Kim, H. C., Lee, J-M., Jeon, Y. & Suh, I. Triglyceride to high density lipoprotein cholesterol ratio among adolescents is associated with adult hypertension: the Kangwha study. Lipids Health Dis. 17, 212 (2018).
Zhang, F. et al. The association of triglyceride and glucose index, and triglyceride to high-density lipoprotein cholesterol ratio with prehypertension and hypertension in normoglycemic subjects: A large cross‐sectional population study. J of Clinical Hypertension [Internet]. 2021 [cited 2023 Dec 24];23:1405–12. Available from: https://onlinelibrary.wiley.com/doi/https://doi.org/10.1111/jch.14305
Wu, Z. et al. Association of TyG index and TG/HDL-C ratio with arterial stiffness progression in a non-normotensive population. Cardiovasc Diabetol [Internet]. [cited 2023 Dec 24];20:134. Available from: https://cardiab.biomedcentral.com/articles/ (2021). https://doi.org/10.1186/s12933-021-01330-6
Thygesen, K. et al. Fourth universal definition of myocardial infarction (2018). J. Am. Coll. Cardiol. 72, 2231–2264 (2018).
Simental-Mendía, L. E., Rodríguez-Morán, M. & Guerrero-Romero, F. The product of fasting glucose and triglycerides as surrogate for identifying insulin resistance in apparently healthy subjects. Metab. Syndr. Relat. D. 6, 299–304 (2008).
Mensah, G. A. et al. Global Burden of Cardiovascular Diseases and Risks, 1990–2022. Journal of the American College of Cardiology [Internet]. [cited 2023 Dec 24];82:2350–473. (2023). Available from: https://www.sciencedirect.com/science/article/pii/S0735109723080233
Yang, H. et al. The relationship between mean arterial pressure and decreased glomerular filtration rate in rural areas of Northeast China. BMC Nephrol. 16, 137 (2015).
Giannini, C. et al. The triglyceride-to-HDL cholesterol ratio: association with insulin resistance in obese youths of different ethnic backgrounds. Diabetes Care. 34, 1869–1874 (2011).
Ormazabal, V. et al. Association between insulin resistance and the development of cardiovascular disease. Cardiovasc. Diabetol. 17, 122 (2018).
Hill, M. A. et al. Insulin resistance, cardiovascular stiffening and cardiovascular disease. Metabolism 119, 154766 (2021).
Mancusi, C. et al. Insulin resistance the hinge between hypertension and type 2 diabetes. High. Blood Press. Cardiovasc. Prev. 27, 515–526 (2020).
Halperin, R. O. et al. Dyslipidemia and the risk of incident hypertension in men. Hypertension 47, 45–50 (2006).
Laaksonen, D. E. et al. Dyslipidaemia as a predictor of hypertension in middle-aged men. Eur. Heart J. 29, 2561–2568 (2008).
Sesso, H. D., Buring, J. E., Chown, M. J., Ridker, P. M. & Gaziano, J. M. A prospective study of plasma lipid levels and hypertension in women. Arch. Intern. Med. 165, 2420–2427 (2005).
Murguía-Romero, M. et al. Plasma triglyceride/HDL-cholesterol ratio, insulin resistance, and cardiometabolic risk in young adults. J Lipid Res [Internet]. [cited 2023 Dec 24];54:2795–9. (2013). Available from: https://linkinghub.elsevier.com/retrieve/pii/S0022227520353050
Tohidi, M., Hatami, M., Hadaegh, F. & Azizi, F. Triglycerides and triglycerides to high-density lipoprotein cholesterol ratio are strong predictors of incident hypertension in middle Eastern women. J. Hum. Hypertens. 26, 525–532 (2012).
Urbina, E. M. et al. Triglyceride to HDL-C Ratio and Increased Arterial Stiffness in Children, Adolescents, and Pediatrics [Internet]. [cited 2023 Dec 25];131:e1082–90. (2013). Available from: https://publications.aap.org/pediatrics/article/131/4/e1082/31844/Triglyceride-to-HDL-C-Ratio-and-Increased-Arterial
Chung, T-H., Shim, J-Y., Kwon, Y-J. & Lee, Y-J. High triglyceride to high-density lipoprotein cholesterol ratio and arterial stiffness in postmenopausal Korean women. J. Clin. Hypertens. (Greenwich). 21, 399–404 (2019).
Ho, C-I. et al. Relationship between TG/HDL-C ratio and metabolic syndrome risk factors with chronic kidney disease in healthy adult population. Clin. Nutr. 34, 874–880 (2015).
Wang, F., Han, L. & Hu, D. Fasting insulin, insulin resistance and risk of hypertension in the general population: A meta-analysis. Clin. Chim. Acta. 464, 57–63 (2017).
Wang, D. et al. Association of the triglyceride-glucose index variability with blood pressure and hypertension: a cohort study. QJM 117, 277–282 (2023).
Wang, K. et al. Association of triglyceride-glucose index and its interaction with obesity on hypertension risk in chinese: a population-based study. J. Hum. Hypertens. 35, 232–239 (2021).
Samuel, P. S., Pociask, F. D., DiZazzo-Miller, R., Carrellas, A. & LeRoy, B. W. Concurrent validity of the international family quality of life survey. Occup. Ther. Health Ca. 30, 187–201 (2016).
Luo, E. et al. High triglyceride-glucose index is associated with poor prognosis in patients with acute ST-elevation myocardial infarction after percutaneous coronary intervention. Cardiovasc. Diabetol. 18, 150 (2019).
Zhang, Y. et al. Predictive effect of triglyceride–glucose index on clinical events in patients with type 2 diabetes mellitus and acute myocardial infarction: results from an observational cohort study in China. Cardiovasc. Diabetol. 20, 43 (2021).
Yu, Y. et al. Combined association of triglyceride-glucose index and systolic blood pressure with all-cause and cardiovascular mortality among the general population. J. Transl Med. 20, 478 (2022).
Wu, Y. et al. Association of mean arterial pressure with 5-year risk of incident diabetes in Chinese adults: a secondary population-based cohort study. BMJ Open. 12, e048194 (2022).
Lee, J. H., Heo, S-J. & Kwon, Y-J. Sex-Specific comparison between triglyceride glucose index and modified triglyceride glucose indices to predict New-Onset hypertension in Middle-Aged and older adults. J. Am. Heart Assoc. 12, e030022 (2023).
De Paoli, M., Zakharia, A. & Werstuck, G. H. The role of Estrogen in insulin resistance: A review of clinical and preclinical data. Am. J. Pathol. 191, 1490–1498 (2021).
Gh, M. D. P. A. Z. W. The Role of Estrogen in Insulin Resistance: A Review of Clinical and Preclinical Data. The American journal of pathology [Internet]. 2021 [cited 2024 Jan 10];191. Available from: https://pubmed.ncbi.nlm.nih.gov/34102108/
Ciarambino, T., Crispino, P., Guarisco, G. & Giordano, M. Gender differences in insulin resistance: new knowledge and perspectives. Curr. Issues Mol. Biol. 45, 7845–7861 (2023).
Somani, Y. B., Pawelczyk, J. A., De Souza, M. J., Kris-Etherton, P. M. & Proctor, D. N. Aging women and their endothelium: probing the relative role of Estrogen on vasodilator function. Am. J. Physiol. Heart Circ. Physiol. 317, H395–404 (2019).
Chang, E., Varghese, M. & Singer, K. Gender and sex differences in adipose tissue. Curr. Diab Rep. 18, 69 (2018).
Kim, S. H., Després, J-P. & Koh, K. K. Obesity and cardiovascular disease: friend or foe? Eur. Heart J. 37, 3560–3568 (2016).
Funding
This work was supported by the National Natural Science Foundation of China (82200500), the Institutional Foundation of the First Affiliated Hospital of Xi’an Jiaotong University (2021QN-03), the Natural Science Foundation of Shaanxi Province, China (2022JQ-787).
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Lele Cheng collected and analyzed data. Yitong Bian and Zixuan Meng analyzed the data. Ping Jin wrote the manuscript. All authors approved the final version to be published and agree to take responsibility for all aspects of the work.
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Cheng, L., Bian, Y., Meng, Z. et al. Association between TG/HDL-C ratio or triglyceride-glucose index and mean arterial pressure in patients with myocardial infarction. Sci Rep 15, 37027 (2025). https://doi.org/10.1038/s41598-025-20158-8
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DOI: https://doi.org/10.1038/s41598-025-20158-8